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J Immunol. 2014 Aug 1;193(3):1314-23. doi: 10.4049/jimmunol.1400089. Epub 2014 Jun 25.

Vitamin D inhibits the occurrence of experimental cerebral malaria in mice by suppressing the host inflammatory response.

Author information

  • 1Department of Immunology, China Medical University, Shenyang 110001, China;
  • 2Department of Immunology, China Medical University, Shenyang 110001, China; Department of Entomology, Pennsylvania State University, University Park, PA 16802; and.
  • 3Department of Immunology, China Medical University, Shenyang 110001, China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001, China;
  • 4Department of Microbiology and Parasitology, China Medical University, Shenyang 110001, China;
  • 5Department of Entomology, Pennsylvania State University, University Park, PA 16802; and.
  • 6Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, PA 16802.
  • 7Department of Entomology, Pennsylvania State University, University Park, PA 16802; and luc2@psu.edu ymcao@mail.cmu.edu.cn.
  • 8Department of Immunology, China Medical University, Shenyang 110001, China; luc2@psu.edu ymcao@mail.cmu.edu.cn.

Abstract

In animal models of experimental cerebral malaria (ECM), neuropathology is associated with an overwhelming inflammatory response and sequestration of leukocytes and parasite-infected RBCs in the brain. In this study, we explored the effect of vitamin D (VD; cholecalciferol) treatment on host immunity and outcome of ECM in C57BL/6 mice during Plasmodium berghei ANKA (PbA) infection. We observed that oral administration of VD both before and after PbA infection completely protected mice from ECM. VD administration significantly dampened the inducible systemic inflammatory responses with reduced circulating cytokines IFN-γ and TNF and decreased expression of these cytokines by the spleen cells. Meanwhile, VD also resulted in decreased expression of the chemokines CXCL9 and CXCL10 and cytoadhesion molecules (ICAM-1, VCAM-1, and CD36) in the brain, leading to reduced accumulation of pathogenic T cells in the brain and ultimately substantial improvement of the blood-brain barriers of PbA-infected mice. In addition, VD inhibited the differentiation, activation, and maturation of splenic dendritic cells. Meanwhile, regulatory T cells and IL-10 expression levels were upregulated upon VD treatment. These data collectively demonstrated the suppressive function of VD on host inflammatory responses, which provides significant survival benefits in the murine ECM model.

Copyright © 2014 by The American Association of Immunologists, Inc.

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